57. Polman CH; Koetsier JC.
[Copolymer 1 in the treatment of multiple sclerosis].
Nederlands Tijdschrift voor Geneeskunde, 1994 Dec 31, 138(53):2636-7.
Language: Dutch.
Pub type: Clinical Trial; Clinical Trial, Phase III; Journal Article;
Randomized Controlled Trial.
130. Bastianello S; Pozzilli C; D'Andrea F; Millefiorini E; Trojano M; Morino
S; Gasperini C; Bozzao A; Gallucci M; Andreula C; et al.
A controlled trial of mitoxantrone in multiple sclerosis: serial MRI
evaluation at one year.
Canadian Journal of Neurological Sciences, 1994 Aug, 21(3):266-70.
Pub type: Clinical Trial; Journal Article; Multicenter Study;
Randomized Controlled Trial.
Abstract: We present the results of a randomized double-blinded placebo
controlled, multicenter trial, of low-dose mitoxantrone (MX), after one
year, in 25 patients with relapsing-remitting multiple sclerosis, who had
serial enhanced magnetic resonance imaging (MRI). Treatment groups were
balanced for age, gender, duration of illness and neurological disability.
Five of the 13 MX patients and 10 of the 12 placebo patients had
exacerbations during treatment (p < 0.02). The mean change in the extended
disability status scale was not significantly different between the MX and
placebo treatment groups. Serial Gadolinium-DTPA enhanced MRI detected no
significant difference between the MX treated and placebo groups in the
mean total number of new, enlarging, or Gadolinium-DTPA enhancing lesions;
there was a trend toward a reduction of new, enlarging and Gadolinium-DTPA
enhancing lesions in MX patients. Despite this ameliorating effect, the
results indicate that serial Gadolinium-DTPA enhanced MRI, performed over
one year in a limited number of patients, could not provide conclusive
evidence for a role of MX therapy in relapsing-remitting multiple
sclerosis.
218. Goodkin DE; Jacobsen DW; Galvez N; Daughtry M; Secic M; Green R.
Serum cobalamin deficiency is uncommon in multiple sclerosis.
Archives of Neurology, 1994 Nov, 51(11):1110-4.
Abstract: OBJECTIVES: To determine the frequency of serum cobalamin (Cbl)
deficiency and to clarify the biologic importance of low screening Cbl
levels in patients with multiple sclerosis (MS) and idiopathic myelopathy
(MYL). BACKGROUND: A significant association between Cbl metabolism and MS
has been postulated based on the observations that patients with MS have
lower serum Cbl levels, higher unsaturated Cbl binding capacities, and a
higher prevalence of macrocytosis than do normal controls. Whether such
observations have biologic importance as documented by abnormal
accumulation of metabolites that would result from Cbl deficiency has not
yet been determined. METHODS: Serum Cbl and folate levels were determined
in 208 consecutively evaluated patients seen in an outpatient MS clinic
setting during a 7-month period. Necessary blood samples were obtained for
165 of these patients. One hundred twenty-five patients had clinically
definite MS, 31 had clinically probable MS, and nine had MYL. Serum
methylmalonic acid (MMA) and homocysteine (HCY) concentrations, which rise
in biologically severe Cbl deficiency, were subsequently determined in all
patients whose Cbl levels were lower than 301 pg/mL. RESULTS: A Cbl level
lower than 301 was found in 32 of 156 patients with either clinically
definite MS or clinically probable MS but in none of the patients with MYL.
Elevated MMA or HCY levels were found in seven of 32 patients with either
clinically definite MS or clinically probable MS, six of whom had an
elevated HCY level and one of urnal Article; Randomized Controlled Trial.
Abstract: 4-Aminopyridine (4-AP) has a favorable effect on the disability of
certain patients with MS. We investigated the effect of 4-AP on
neuropsychological performance in 20 MS patients using a randomized,
double-blind, placebo-controlled, crossover design. Although there was a
trend for improved performance with 4-AP for two ofing to a randomized, double-blind,
double-crossover design. MAIN OUTCOME MEASURES: Neurophysiologic variables
for nonresponders, neurologic functions and symptoms on a visual analogue
scale for responders, and side effects for both groups. RESULTS: Toxicity
profiles of 4-aminopyridine and 3,4-diaminopyridine were different, and
systemic tolerability was reduced for 3,4-di44(11 Suppl 9):S34-42; discussion S42-3.
Pub type: Clinical Trial; Journal Article; Multicenter Study;
Randomized Controlled Trial.
Abstract: This multicenter, stratified, randomized, placebo-controlled,
double-blind trial evaluated tizanidine for use in the United States for
spasticity secondary to MS. The 15-week trial was divided into baseline
(weeks 0 atnd
physician/prescribers, but not physician/assessors, gave significantly
better scores in the overall assessment of efficacy and tolerability. No
significant differences in other secondary efficacy parameters were noted.
Adverse events were reported for 66 (61%) of the 109 placebo-treated
patients and 101 (91%) of the 111 tizanidine-treated patients; 6 (6%) and
14 aticity f h lgsdu omutilescerss.A
rms smuscle one knee exensrs,
appying Wartenberg's pendulum test. Blood samples, a clinical assessment
of muscle tone by the Ashworth scale, and muscle strength by the British
Medical Research Council scale were obtained concomitantly. Confirmatory
analysis using the change in the relaxation index (R2 value) 1.5 hours
after each treatment,ceboontrolled trial of tizanidine in the treatment of
spasticity caused by multiple sclerosis. United Kingdom Tizanidine Trial
Group.
Neurology, 1994 Nov, 44(11 Suppl 9):S70-8.
Pub type: Clinical Trial; Journal Article; Multicenter Study;
Randomized Controlled Trial.
Abstract: Tizanidine was evaluated in a prospective, double-blind, randomized,
r
eas 1 eek aterdisontiutionof herp. A arity of adverse events
was recordytn agini thee n d rei,dallietae ade e-lad dfcerf symptomaticttnostc
265. Miller DJ; Sanborn KS; Katzmann JA; Rodriguez M.
Monoclonal autoantibodies promote central nervous system repair in an
animal model of multiple sclerosis.
Journal of Neuroscience, 1994 Oct, 14(10):6230-8.
Abstract: Susceptible strains of mice infected intracerebrally with Theiler's
murine encephalomyelitis virus develop a chronic, progressive,
immune-mediated CNS demyelinating disease similar both pathologically and
clinically to multiple sclerosis. Previous reports indicated that
polyclonal immunoglobulins from mice injected with homogenized spinal cord
promote CNS remyelination when given to SJL/J mice chronically infected
with Theiler's virus. To explore further both the mechanism(s) and
potential therapeutic usefulness of antibodies in the treatment of CNS
demyelinating diseases, we made a panel of monoclonal antibodies derived
from splenocytes of SJL/J mice injected with homogenized spinal cord, and
screened them for their autoantigen-binding capability. Monoclonal IgM
autoantibodies from two clones, designated SCH94.03 and SCH94.32, promoted
fourfold more CNS remyelination than controls when given to chronically
infected SJL/J mice. CNS remyelination, assessed morphologically by the
presence of abnormally thin myelin sheaths relative to axonal diameter,
correlated with the absence of clinical disease progression. In titration
experiments, treatment with SCH94.03 and remyelination had a positive
dose-response relationship, and as little as 10 micrograms of antibody
promoted remyelination. Both SCH94.03 and SCH94.32 showed multiorgan
autoreactivity, and recognized both surface and cytoplasmic determinants on
glial cells. We propose that this model provides a unique system to
elucidate the mechanism(s) and test the reparative potential of
autoantibodies in the treatment of CNS injury.
302. Nieves J; Cosman F; Herbert J; Shen V; Lindsay R.
High prevalence of vitamin D deficiency and reduced bone mass in
multiple sclerosis.
Neurology, 1994 Sep, 44(9):1687-92.
Abstract: BACKGROUND: Female patients with multiple sclerosis (MS) are at risk
for osteoporosis because of gender, immobility, and corticosteroid use.
METHODS: Bone mineral density (BMD) was measured by dual x-ray
absorptiometry in 80 female MS patients admitted to a tertiary care
hospital. All patients completed a questionnaire that included measurements
of dietary intake and sunlight exposure. Biochemical indices of bone
metabolism and turnover were measured in a random sample of 52 patients.
RESULTS: BMD of the lumbar spine and femoral neck was 1 to 2 SDs lower in
MS women compared with a healthy reference population. BMD was lower in
patients with more severe MS. The mean 25(OH)D level of the sample
population (43 nmol/l) was in the insufficient range, and 12 patients (23%)
had frank vitamin D deficiency (< 25 nmol/l). BMD and age-related BMD (z
scores) at all skeletal sites measured were lowest when 25(OH)D levels were
deficient. Parathyroid hormone (PTH) was frankly elevated in 13% of
patients. PTH levels were negatively correlated with 25(OH)D levels and
with BMD. Dietary intake of vitamin D was below the recommended level in
80% of patients, and 40% reported no weekly sunlight exposure. After
controlling for age, cumulative steroid use was not a determinant of BMD.
CONCLUSIONS: BMD was significantly reduced in female MS patients, which
might increase fracture risk two- to threefold. Vitamin D deficiency with
secondary hyperparathyroidism is prevalent and is probably a significant
cause of low BMD in this population. Vitamin D deficiency in the female MS
patient might be safely and inexpensively corrected by the routine use of
vitamin D supplements.
312. Polman CH; Koetsier JC.
Cladribine treatment of multiple sclerosis [letter].
Lancet, 1994 Aug 20, 344(8921):537; discussion 537-8.
Pub type: Letter.
314. Grieb P; Ryba M; Stelmasiak Z; Nowicki J; Solski J; Jakubowska B.
Cladribine treatment of multiple sclerosis [letter].
Lancet, 1994 Aug 20, 344(8921):538.
ct from injury
cells which they support during development, there should soon be
opportunities for limiting damage following a variety of insults and for
rescuing degenerating neurones and glia. The discovery that axon
regeneration is actively inhibited, perhaps in order to maintain stability
in the complex systems and circuits that are established during
developmentain rpair strategy but ta rv pssible to restore complex
cellular arrangements through cell implantation only. Grafted neurones
survive, produce appropriate neurotransmitters, form connections and
restore some behaviours, but their relative inability to grow limits the
degree of structural and functional repair that can be achieved:
nevertheless, nerve cell implantation isctile dysfunction (SCI, 14; multiple sclerosis, 7;
discogenic disease, 6) were evaluated and treated with intracavernous
PGE-1. An average of 3.2 office sessions were required to learn adequate
self-injection technique and deeie otmal dosage require. ntil
dsag frSCmewas 2.5 micrograms and increased in 2.5 micrograms
increments to a mean maintenance dos of6.micrgrams Quartrlyodaarpisi mcriio pdmen thtbia
orialevoked potentials. The neurological examination findings together
with the results of the neurophysiological and cystometric tests suggest
that erectile dysfunction in multiple sclerosis is due to spinal lesions
situated proximal to the sacral cord. The feasability of papaverine
intracorporeal injection therapy for men with multiple sclerososis brains that remyelination can occur
after the myelin damage. This myelin repair is achieved by
oligodendrocytes, which are the myelinating cells of the central nervous
system or by oligodendrocytes precursors still present in adult central
nervous system. Several recently discovered growth factors can stimulate
oligodendrocytes precursors migration and proliferation, Neurology, 1994 Oct41: Pub type: Letter.
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